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Pathology > Cell Injury: Sub-lethal and Lethal Injury > Flashcards

Cell Injury: Sub-lethal and Lethal Injury Flashcards

1
Q

Does the need for blood supply change in cell when performing exercise?

A

Yes! Significantly! The harder the exercise, the higher the demand for blood.

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2
Q

Cause of Cell Death - Ischemia

A

Insufficient blood supply die to decrease in blood flow or increased metabolic function.

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3
Q

Hypoxia

A

Partial obstruction of O2

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4
Q

Anoxia

A

Complete obstruction of O2

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5
Q

Drowning

A

Obstruction of the respiratory tree

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6
Q

Pneumonia

A

Inadequate O2 transport across lung surface

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7
Q

Anemia

A

Lack of RBCs to transport O2 in the blood

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8
Q

CO Poisoning

A

Inability of cell to use O@ for cellular respiration

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9
Q

What happens with decreased blood flow?

A

Decreased O2 supply, changes metabolism from aerobic to anaerobic
Decreased ATP synthesis changes cell membrane permeability and can lead to intracellular movement of ions and fluids. Results in cell swelling (Na+ comes in and brings water with it) and affects cellular homeostasis.
Increased build up of O2
Results in cell death (necrosis) if not reversed

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10
Q

Causes of Cell Death - Infecting Agents

A

Bacteria and Viruses

Exotoxin

  • Come inside and secrete something
  • Ex: Snake bite with venom

Endotoxin
-Cell wall gets destroyed, wall has toxins inside of it which go to other areas of the body and cause issues.

Infecting agents can cause inflammation/immune reactions of the body that damages cells/tissues

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11
Q

Example of Exotoxins (2)

A

Botulinum: Destroys SNARE proteins (can’t bring ACh in)

Tetani: Blocks GABA and glycine NTs - inhibitory NTs

Leads to increased muscle contractions in both examples

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12
Q

Example of Endotoxin

A

Sepsis: Loss of plasma volume, hypovolemic, endothelial cell damage

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13
Q

What are the two ways viruses can kill?

A

Direct and Indirect

Direct Crytopathic effect: Invades and redirects cell machinery and disturb the cell

Indirect Cytopathic effect:

Hijack our DNA to make RNA by going into cell changing the enzyme to create DNA to RNA that’s sent out and causes injury

Viral proteins insert on the cell membrane -> form pores -> alter cell permeability -> cell swelling and death

Viral proteins integrate into cellular genome -> produces foreign proteins -> encodes proteins are expressed on the cell surface -> T lymphocytes recognize this foreign protein -> attacks and destroys host cells

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14
Q

Cause of Cell Injury - Immune Reactions

A

Cell injury -> Antigen -> Inflammatory Cells ( Neutrophils, Macrophages, T and B Lymphocytes) -> IgE antibodies on the surface of Mast and Basophils (releases histamines)

Mild reaction: Runny and watery eyes

Moderate to severe: Bronchoconstriction

Cross-reactivity between foreign antigen and host antigen
-Something nonself and self

Chronic persistence of foreign antigens
-Chronic inflammatory reaction

Sensitization to endogenous antigens (Type 1 DM)
-Viral infection -> islet antigens -> destruction of islet cells by T cells

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15
Q

Cell Injury - Chemical Factors

A

Directly injure cells: Mercury

Metabolically transformed into toxic agents - acetaminophen

Oxygen toxicity phenomenon: Normal cellular metabolism for energy produces free electrons (steals electron from healthy cells) + oxygen + hydrogen for stability = ROS

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16
Q

What is ROS?

A

Reactive Oxygen Species

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17
Q

Factors that likely increase oxygen toxicity

A

Prolonged and intense exercise (sedentary), prolonged exposure to high levels of oxygen, UV light, pollutants, tobacco smoke, poor nutrition

Conditions: HEart Disease, CVA, Diabetes mellitus, Parkinsons Disease, Alzheimers, Premature aging and cancer

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18
Q

Are all radicals bad?

A

No! Some are positive helping fight inflammation, kill bacteria, regulate ANS

Enzymes in cells converts radicals back to usable oxygen

Ex: Nitric Oxide is good!

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19
Q

Why are antioxidants important?

A

Neutralize free radicals and protects cells/DNA from damages

Endogenous and Exogenous

20
Q

What are some benefits from NO?

A

Long term memory
Increases cell membrane permeability (easy crossing of ACh)
Helps GI mucosa
Inhibits virally induced cytokine and chemokine production
Stimulates collagen synthesis

Anti-lipid: coats blood vessels
-Helps prevent platelet adhesion and promotes fibrinolysis

21
Q

Exercise and Free Radicals

A

Moderate, regular long-term aerobic exercise protects DNA damage

Increase formation of NO
Up-regulation of endogenous antioxidants

22
Q

FITT

A

Frequency
Intensity
Time
Type

23
Q

What is the recommended exercise dosage?

A

At least 150 min of moderate-intensity aerobic activity

At least 2 days of muscle-strengthing activity

24
Q

Causes of Cell Injury - Genetic Factors

A

Alterations in structure or number of chromosomes

25
Q

Causes of Cell Injury - Mechanical Factors

A

Physical stress theory

Changes in the relative level of physical stress cause a predictable adaption

Typical Response:
Death
Injury
Maintenance
Atrophy (Decreased Stress Tolerance)
Hypertrophy (Increased Stress Tolerance)

26
Q

Cell Injury - Nutritional Factors

A
  • Nutritional Imbalances – abnormal vitamins and mineral
  • Lack of essential amino acids affects protein synthesis
    • Deficiency: Protein malnutrition (Kwashiorkor), Marasmus (generalizaed deficency)
    • Excessive: Obesity
    • Decreased iron – leads to anemia
    • Increased iron (hemochromatosis) - forms free radiaclas and damages cell/tissues/organs
  • Think about athletes and iron deficiency/excess iron
    • Female athletes and menstration
27
Q

Fatty Liver

A
  • Alcohol: Liver produces lots of lipids and no protein lead to injury
    • Proteins are needed to transport fat in the blood from liver
  • Increase in intracellular lipid accumulation within hepatocytes as tissues overload or form various metabolites
28
Q

CI - Physical Injuries

A
  • Trauma – motor vehicles accidents and penetrating trauma by weapons – prolonged rehabilitation
  • Extremes of physical agents:
    • Temperature: Hypothermia and hyperthermia
    • Electricity
  • Irradiation
    • Radiolysis of water and production of hydroxyl radicals -> membrane damage and breakdown of structural and enzymatic proteins results in cell death
    • Damage to arterioles -> inadequate blood supply (ischemia) to irradiated tissues
    • Damage to nucleic acids leads to gene mutations
29
Q

CI - Psychosocial Factors

A

Fear, tension anxiety – influence individual threshold for tissue adaptation and injury

Occasionally satisfied or unsatisfied work environment -> higher risk of injury

30
Q

Cellular Aging

A

Aging and Aging-related changes significantly affect homeostasis and the recovery process

>300 theories to explain cellular aging

Telomere aging clock

Telomere on chromosomal end decreases. Without telomere the cell dies.

Trying to stop this process may lead to cancer

31
Q

Cell Injury

A

Ionic shifts across cell membrane with increased sodium and calcium influx into cell

Increased cell volume (swelling) in cytosol – mitochondria, ER

Increased lactic and anerobic metabolism, increased pH

Go from anerobic to aerobic system

Don’t reduce stress leads to death

32
Q

Cellular Adaptations - Atrophy

A
  • Atrophy – reduction in cell size (not number) and organ size
  • Other Examples: Muscle wasting, bone loss, spinal atrophy in spinal cord injury
  • Cachexia in cancer die to diet and malnutrition
    • Loss of muscle and fat
    • Focus on doing what patient can do at that time, don’t push them
33
Q

CA – Hypertrophy

A
  • Hypertrophy – increase in cell size and organ size
    • Pure hypertrophy occurs in striated muscles (heart and skeletal muscles)
      • Ex: Left ventricle hypertrophy
    • Hypertension due to increased blood pressure causes hypertrophy
34
Q

CA-Hyperplasia

A
  • Hyperplasia – increase in number of cells -> organ size
    • Ex: Caluses on hands from weight lifting
  • Pure hyperplasia: endometrial thickness and callus
  • Hypertrophy and hyperplasia occur together in prostate enlargement, obstruction of the urethra and bladder
35
Q

Metaplasia

A
  • Metaplasia – change in cell morphology and function. One adult cell type to another
    • Ex: Smoking
      • Changes from ciliated psuedostratisfied columnar to stratisfies squamous epithelium
        • Leads to thickening of respiratory epithelium
        • If smokers stop cells can regenerate back to normal
36
Q

Dysplasia

A
  • Increase in cell numbers, altered cell morphoplogy and loss of histologic organization
    • Usually seen in cancer patient
    • Neoplasia and aplasia
      • Neoplasia: Cancer
      • Aplasia: Cell is abnormal; Origin is unknown
37
Q

Can the cell revert to normal?

A

If the nucleus is not damages

Remove stress

Restore energy source

Restore ion balance

38
Q

Necrosis

A
  • Necrosis: Cell Death when exposed to uncontrolled extreme conditions
    • Internal cellular environment leads to complete discord to cell functioning
    • Wall or membrane of cell
    • Leads to inflammation
    • Disintegration
    • Passive, No energy required
    • Enlarged
    • Lysosomes and mitochondria release cells that lead to cell death
      • Mitochondria
        • Leads to aerobic to anerobic shift
39
Q

Apoptosis

A
  • Apoptosis: Preplanned cell death, cell takes part in its death
    • Die naturally, Ex: RBCs live for 120 days
    • If cells don’t die on time leads to cancer
    • Cells die to fast leads to heart disease, liver disease, AIDs
    • No disintegration
    • Shrinkage of cell
    • Requires Energy
40
Q

Hallmarks of Lethal Injury

A
  • Nucleus
  • Mitochondria: decreased ATP and energy production
  • Lysosomes: decrease digestive enzymes after death
  • Dead cells are released into ECF and then into circulation (clinical markers of injury)
    • Biomarkers can be released in system and tested to see if there are issues
    • Ex: C-Reactive Protein
41
Q

Coagulative (Dry Gangrene)

A
  • Coagulative (dry gangrene) - several days after cell death
  • Ischemia
  • Liver
42
Q

Liquefactive (wet gangrene)

A

Liquefactive (wet gangrene) - within hours of cell death

Bacteria

Brain

43
Q

Gangrenous Necrosis

A

Extremities

44
Q

Caseous Necrosis

A

TB

Granuloma

Protective cells make a wall around bacteria

45
Q

Fatty Necrosis

A

Abdomen region

46
Q

Fibrinoid necrosis

A

Trauma in blood vessel wall

47
Q

Gas Gangrene

A

Pathogen: Clostridium Perfringens

Blisters with gas bubbles of the affected area, fever, pain, increased Hr/breathing

Ex: Surgery, cellulitis, fasciitis

Pathology (7 decks)

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